Cough Flashcards

Question

How do we diagnose bronchiolitis?

Answer 1

- Usually clinical 1. CXR – hyperinflation with patchy atelectasis, peribronchial infiltrates. NOT routinely indicated if uncomplicated 2. ABG – if severe, assess acidosis

Answer 2

supportive

Answer 3

1. Based on severity a. Mild – home mgt. Inc OFI, bronchodilator not recommended b. Severe – ventilatory & O2 support (cool humidified O2 for hypoxemic px), hydration, Ribavirin - Not recommended: bronchodilators, chest PT, CS, abx, epi 2. Admission: a. Marked respiratory distress (nasal flaring, retractions, tachypnea, dyspnea, cyanosis) b. Age <12 w c. Toxic appearance, poor feeding, dehydration, lethargy d. Apnea e. O2 sat <92% f. Hx of prematurity g. Comorbidity CV, pulmo, neuro, immune h. Unreliable caregivers 3. Mgt if hospitalized: nebulized hypertonic saline (3%) 2.5-3ml prn 4. Prevention a. Palivizumab (monoclonal Ab) for <2yo w/ CHD b. Hand hygiene c. Exclusive bf x 6 mos

Answer 4

inflammation of lung parenchyma

Answer 5

Etiology: 1. Neonates (0-28d) – GBS, E.coli, Listeria, S.pneumonia, HiB 2. 3w-3mos – RSV, parainfluenza, chlamydia trachomatis, M.pneumoniae, S.pneumoniae, Hib, S.aureus 3. 4m-4yo – RSV, S.pneumoniae, HiB, M.pneumoniae 4. >5yo – M.pneumoniae, S.pneumoniae, Chlamydia pneumoniae (atypical PN)

Answer 6

S. pneumoniae

Answer 7

- Trauma, anesthesia, and aspiration increase the risk of pulmonary infection - Viral PN: results from spread of infection along the airways + direct injury of the respiratory epithelium à airway obstruction from swelling, abn secretions, and cellular debris à atelectasis, interstitial edema, VQ mismatch à significant hypoxemia - Bacterial PN: bacteria colonizes trachea and enter lungs, or from direct seeding of lungs after bacteremia Mycoplasma – viral MOA à inhibits ciliary action, cellular destruction à airway obstruction S.pneumoniae – local edema allowing bacterial proliferation and spread into adjacent lung portions à focal lobar involvement GAS – diffuse infection with interstitial PN. Necrosis of tracheobronchial mucosa, formation of large amounts of exudate, edema, and local hemorrhage, extension into the interalveolar septa à involvement of lymphatic vessels and pleural involvement S.aureus – confluent bronchoPN (unilateral), extensive hemorrhagic necrosis, irregular areas of cavitation in the lung parenchyma à pneumatocoeles, empyema, bronchopleural fistulas

Answer 8

CM: 1. Clinical triad: fever, cough, tachypnea 2. Abdominal pain – lower lobe PN 3. Tachypnea – most consistent 4. Early – diminished BS, scattered crackles and rhonchi 5. Late – dullness on percussion, chest lag/asymmetrical chest on affected side (from consolidation/pleural effusion) 6. Respiratory failure – retractions, head bobbing, cyanosis, grunting, apnea, changes in sensorium 7. Recurrent PN - >2 episodes in a single year or >3

Answer 9

Dx: 1. CXR (PAL) – lung infiltrates. Complications such as pleural effusion or empyema - Viral PN: hyperinflation with bilateral interstitial infiltrates and peribronchial cuffing - Pneumococcal, atypical PN: confluent lobar consolidation - Bacterial: pleural effusion, lobar consolidation 2. Pulse oximetry 3. GS, C/S of sputum, nasopharyngeal aspirate, pleural fluid &/or blood – definitive Dx for bacterial PN 4. BCS – only (+) in 10% of pneumococcal PN. Not recommended for non-severe OPD cases. Recommended for severe, clinical deterioration, complicated PN 5. Chest UTZ -if suspecting multi-lobar consolidation, necrotizing PN, lung abscess, pleural effusion, air leak 6. ABG 7. CBC – WBC N or elev (viral: <20K, bact 15-40K), lymphocyte predominance (viral), granulocyte predominance (bact) 8. CRP, ESR procalcitonin (marker of bacterial pathogen) – elev in pneumococcal PN 9. PCR (+) – for M.pneumoniae

Answer 10

PCAP A or B – abx administered if: a. >2yo b. With HG fever without wheeze PCAP C – empiric abx may be started if any of the ff is present: a. Elevated serum CRP, PCT, WBC >15k, Lpc-2 b. Alveolar consolidation on CXR c. Persistent HG fever without wheeze PCAP D – refer to specialist PCAP A/B 1. Complete HiB vax: Amoxcillin 80-90 mkd q12 po x 5d 2. No/incomplete HiB vax: Co-amoxiclav 80-90 mkd po q12/ Cefuroxime 20-30 mkd po q12 3. Allergy: Azithromycin 10mkd po x 3d or 10mkd po on D1 then 5mkd po on D2-4/ Clarithromycin 15mkd po q12 x 7d 4. If non-responsive to initial tx (48-72h): Shift Amoxicillin to Co-amoxiclav 90mkd po q12 If started on Co-amox, Admit for IV abx + macrolide po PCAP C 5. Complete HiB vax: Penicillin G 200,000 U/k/d IV q6 Ampicillin 200mkd q6 IV 6. No HiB vax: Ampicillin-Sulbactam 100mkd q6 / Cefuroxime 10mkd IV 18/ Ceftriaxone 100mkd q12 IV PCAP D: refer to Pulmo/ ID Atypical PN, >5yo/adolescents - Azithromycin 10mkd OD x 3 d Clarithromycin 15mkd BID x 10d Erythromycin 50mkd po q6-8 po 7. Adolescent: FQ: Ciprofloxacin 20-30mkd po q12. Caution for <18yo. Reserve for complicated cases. Why? Due to possible arthrotoxicity. 8. >15yo: Ampicillin-sulbactam 100-200 mkd IV q6h Cefuroxime 20-30mkd po, 75-150 mkd q8 IV carbapenem + macrolide/FQ Ceftriaxone 2g IV OD x 7d + Azith 500mg ODx5d Staphylococcal: Clindamycin 10-30mkd po q6-8h, 25- 40mkd IV q6-8h 9. MRSA: Vancomycin 45-60 mkd q6-8h IV

Answer 11

Complications: From direct spread/bacteremia - Pleural effusion/empyema – S.aureus, S.pneumonia, S.pyogenes – most common - Pericarditis - Meningitis - Suppurative arthritis - Osteomyelitis - Vaccines: influenza, PCV13

Answer 12

Epidemiology: - Choking – leading cause of morbidity and mortality in <4yo - Most common: food, coins, balloons, toys - Food: peanuts, carrot, apple, dried beans, popcorn, sunflower, watermelon seeds, hard candy, chewing gum, hotdog, grapes (globular-shaped) - AAP: recommends children <5yo should avoid hard candy, gum; raw fruits and vegetables to be cut into smaller pieces

Answer 13

Due to underdeveloped ability to swallow food, smaller diameter airway more prone to obstruction, less force of air during coughing

Answer 14

CM: 1. Initial event: violent paroxysms of coughing, choking, gagging, new-onset wheezing new-onset wheezing 2. Asymptomatic interval: FB lodged, reflexes fatigue, sx subside. Most treacherous stage. Account for delayed dx. 3. Complications: Complete airway obstruction – most serious complication. Sudden respiratory distress followed by inability to speak/cough Erosion, infection: fever, cough, hemoptysis, PN, atelectasis

Answer 15

Dx: - Clinical dx 1. Bronchoscopy – done ASAP once with strong suspicion - Usually R bronchus (58%), larynx or trachea (10%) 2. CT scan – define radiolucent FB (fish bone) 3. PA and lateral neck XR – if tracheal 4. PA & lateral CXR – If bronchial. Obstructive emphysema, air trapping, shift of mediastinum towards opposite side - The hallmark of an aspirated foreign body is a lung volume that does not change during the respiratory cycle - due to the check valve mechanism, where air enters the bronchus around the foreign body but cannot exit, the affected lung will usually appear overinflated and hyperlucent, with concomitant rib flaring and a depressed ipsilateral hemidiaphragm - interrupted bronchus sign: disruption of the air column in the main bronchi - the majority of foreign bodies are radiolucent

Answer 16

Mgt: 1. referral to Pulmonology for prompt endoscopic removal of FB 2. Heimlich maneuver – if laryngeal FB

Answer 17

Laryngotracheobronchitis (LTB)

Answer 18

Parainfluenza

Answer 19

Acute inflammatory disease of the larynx (within the subglottic space) - The infection causes inflammation of the larynx, trachea, bronchi, bronchioles, and lung parenchyma. Obstruction caused by swelling and inflammatory exudates develops and becomes pronounced in the subglottic region. Obstruction increases the work of breathing.

Answer 20

subglottic

Answer 21

1. URTI and LG fever 1-3 d prior to upper airway obstruction (prodrome 1-7d) 2. “barking cough” 3. Hoarse voice 4. Sx worse at night 5. Coryza & rhinorrhea 6. N to moderately inflamed pharynx 7. Slight tachypnea 8. Inspiratory stridor (on exertion if mild, at rest for modsevere)

Answer 22

1. Clinical Westley croup score 2.Neck xray: steeple sign/subglottic narrowing 3. Endoscopy-definitive; deep red mucosa and subglottic edema 4. CBC- usually nonspecific. WBC N or low with lymphocytosis

Answer 23

Steeple sign

Answer 24

Dx: 1. Clinical 2. Neck XR – steeple sign/subglottic narrowing: the narrowing of airway lumen alters the appearance of tracheal air column, which resembles a church steeple or a steeply pitched roof. - Do not correlate with ds severity 3. Endoscopy – definitive; deep red mucosa and subglottic edema 4. CBC – usually nonspecific. WBC N or low with lymphocytosis. Mgt: 1. Admission criteria: a. Severe ds: poor air entry, altered consciousness b. Deterioration after initial medical management c. Severe dehydration d. Fx suggesting secondary bacterial infection 2. Discharge criteria: a. No stridor at rest b. N O2 sat c. Good air exchange d. No cyanosis e. N level of consciousness f. Able to tolerate fluids by mouth 3. Mild: Dexamethasone 0.6mkdose, Budesonide 2mg neb 4. Moderate to severe: a. Dexamethasone 0.6mkdose b. Humidified oxygen (if O2sat <92%) c. NPO d. Nebulize epinephrine x 15 min (0.5ml/kg/dose using 1:1000 dilution, max 5ml) 5. Impending respiratory failure: a. High O2 using nonrebreathing mask b. Dexamethasone c. ET intubated

Answer 25

medical emergency; serious, acute, rapidly progressive infection of supraglottic structures

Answer 26

HiB in unvaccinated children S.pyogenes, S. pneumoniae, S. aureus in vaccinated

Answer 27

Pathophysio - Hib infection of the epiglottis leads to acute onset of inflammatory edema, beginning on the lingual surface of the epiglottis where the submucosa is loosely attached. Swelling significantly reduces the airway aperture. Edema rapidly progresses to involve the subglottic structures (aryepiglottic folds, arytenoids, and entire supraglottic larynx). The tightly bound epithelium on the vocal cords halts edema spread at this level. Frank airway obstruction, aspiration of oropharyngeal secretions, or distal mucous plugging can cause respiratory arrest.

Answer 28

CM: 1. Acute onset (4-12h) of HG fever, severe sore throat, dyspnea, rapidly progressing respiratory obstruction 2. Dysphagia, drooling, hyperextended neck to maintain airway, muffled voice, sniffing dog or tripod position 3. Double set-up PE (risk of airway obstruction and respiratory arrest: direct visualization of inflamed cherry-red epiglottis (Hib) or pale and edematous epiglottis (Streptococcus) 4D’s: Dysphagia, Dysphonia, Drooling, Distress

Answer 29

Dx: 1. C/S – blood, epiglottic surface, CSF 2. CBC – leukocytosis with neutrophilia 3. ABG – respiratory acidosis 4. Lateral neck XR – thumb/ thumbprint/ leaf sign: thickened free edge of the epiglottis, which causes it to appear more radiopaque than normal, resembling the distal thumb 5. Fiberoptic laryngoscopy – direct visualization of cherry red epiglottis

Answer 30

Mgt: 1. Intubation/tracheostomy under double set-up – 1st priority. Ave 1-3 d - Extubate when air leak develops around tube 2. Abx x 7-10d 1st line: Ceftriaxone 50-75 mkd IV q12/24 2nd line: Ampicillin-Sulbactam 100mkd IV q6 x 10d Alt: Cefotaxime 100-200 mkd IV q6-8h Meropenem 60mkd IV q8

Answer 31

Prophylaxis: Rifampicin 20mkd po OD x 4 d for all household members with: 1. Any contact <4yo incompletely immunized 2. Any contact <12 mo w/o any primary vaccination 3. All immunocompromised

Answer 32

meningitis, otitis media, PN, cellulitis

Answer 33

S. aureus Others: MRSA, S.pneumonia, S.pyogenes, M.catarrhalis, nontypeable H.influenzae, anaerobes - Age: 6mos-8yo (peak 5-7yo)

Answer 34

Site: trachea - mucosal damage or impairment of local immune mechanisms due to a preceding viral infection, an injury to the trachea from recent intubation, or trauma may predispose the airway to invasive infection with common pyogenic organisms.

Answer 35

1. Slow onset with sudden deterioration. Often follow viral URTI 2. Brassy cough, hoarse voice 3. HG fever and toxicity can occur immediately or after a few days of apparent improvement 4. Stridor, neck pain 5. Can lie flat, does not drool, no dysphagia 6. Mucosal swelling at the level of the cricoid cartilage with copious thick, purulent secretions

Answer 36

Dx: 1. Clinical – r/o epiglottitis 2. Neck XR – ragged/hazy tracheal column, pseudomembrane detachment from soft tissues in the trachea (lateral view) 3. Bronchoscopy – subglottic narrowing, diffuse erythema and mucopurulent exudates that may partially occlude the airway. 4. Blood C/S, CBC – N or elev WBC, inc in immature cells on diff count

Answer 37

Mgt: 1. Vancomycin/clindamycin + 3rd gen cephalosporin (Ceftriaxone, Cefotaxime) Vancomycin 40-46 mkd IV q6-8 Clindamycin 25-40 mkd IV q6-8 Ceftriaxone 50-75 mkd IV q12-24 Cefotaxime 100-200mkd IV q6 2. Intubation (50-60%)

Answer 38

- A reversible, obstructive, airway disease involving both the small & large airways with increased residual lung volumes and decreased FEV1/FVC ratio

Answer 39

- 3 components of an asthma attack: § Bronchospasm § Airway edema § Increased mucus production - Hypersensitivity or susceptibility to exposures/triggers lead to airway inflammation, airway hyperresponsiveness, edema, basement membrane thickening, subepithelial collagen deposition, smooth muscle and mucous gland hypertrophy, and mucus hypersecretion --> airflow obstruction

Answer 40

CM: 1. Wheezing, SOB, chest tightness, cough 2. Sx worsen with certain “triggers” (viral infection, weather changes, exercise, allergen, emotions, stress) 3. Responds to bronchodilators 4. (+)FHx of asthma or atopy

Answer 41

Asthma Predictive Index (API) – >4 wheezing episodes per year + 1 major criteria or 2 minor criteria - Major criteria: Physician diagnosed atopic dermatitis in the child, physician diagnosed asthma in a parent, sensitization to an inhalant - Minor criteria: wheeze apart from cold, eosinophilia, sensitization to food Perform spirometry/PEF with BD reversibility test Daily diurnal PEF variability = twice daily PEF [(day’s highest-day’s lowest]/mean of day’s highest and lowest) x 100, averaged over one week

Answer 42

Diagnosis in Children <5yo: - PFT not done due to inability to correctly perform maneuvers - Clinical. CXR to r/o structural abnormality - Fx suggestive of asthma: § Recurrent or persistent non-productive cough worse at night § Recurrent wheezing during sleep or exposure to triggers § Reduced activity § Therapeutic trial with low dose ICS & prn SABA results in clinical improvement in 2-3 mos & worsening when tx is stopped. Asthma severity is assessed retrospectively, q2-3 mos of treatment.

Answer 43

Low FEV1 – (<60% predicted) identifies patients at risk of asthma exacerbations, independent of Sx N or near N FEV1 – consider alternative causes Persistent BD reversibility – increase in FEV1 >12% and >200ml from baseline = uncontrolled asthma Spirometry – cannot be readily obtained in children <5yo After starting ICS Tx, FEV1 improves then reaches a plateau after 2mos --> personal best FEV1 (highest FEV1) should be recorded - Better predictor in clinical practice - Personal best PEF is reached after 2 weeks Excessive variation in PEF suggests poor asthma control, high risk of exacerbation.

Answer 44

2020 GINA Updates 1. Maximum daily dose for formoterol is 48mcg (w/ beclomethasone) and 72mcg (w/ budesonide) 2. Use of ICS for step 1 in children 6-11yo 3. Definition of low, medium, and high dose ICS revised to reflect clinical use 4. Alert on risk of monteleukast adverse effects (aggression, insomnia, anxiety, hallucinations, depression, suicide) 5. Assessment criteria for severe attack in children <5yo revised A. Pharmacologic therapy * 3 Main categories: 1. Controller medications – reduce airway inflammation, control sx, reduce exacerbations and decline in lung function 2. Reliever/rescue medications – prn relief of breakthrough sx (worsening asthma/ exacerbations. Short term prevention of exercise induced bronchoconstriction. 3. Add-on therapies for severe asthma – considered if with persistent sx despite optimized tx. SMART regimen – Single Maintenance and Reliever Tx Asthma treatment is a continuous cycle: - Assess, adjust treatment, and review response Assess for common problems: - Inhaler technique - Adherence - Persistent allergen exposure and comorbidities

Answer 45

Ideally, patients should be seen 1-3 months after starting treatment and q3-12 months thereafter. After an exacerbation, a review visit within 1 week should be scheduled. After starting initial controller, review response after 2-3 mos (or according to urgency) - Consider stepping down: § once good control has been achieved and maintained for 3 months, low risk for exacerbations. - Consider Stepping up: § Uncontrolled sx, exacerbations or risk 1. Sustained step-up (for at least 2-3 mos) 2. Short term step-up (for 1-2 weeks) – for viral infections or seasonal allergen exposure. Find the patient’s lowest treatment that controls both sx and exacerbations. B. Non-pharmacologic therapy 1. Cessation of smoking for patients, parents or caregivers 2. Healthy diet and regular exercise, weight reduction 3. Avoidance of triggers/allergens, pollution 4. Avoidance of meds that may make asthma worse (aspirin, NSAIDs, beta-blockers) 5. Immunizations (Influenza, pneumococcal vax) 6. Provide written asthma action plan

Answer 46

Interim guidance during COVID-19 pandemic 1. Continue ICS and OCS as prescribed 2. All patients should have asthma action plan 3. Avoid use of nebulizers if possible a. Viruses can be transmitted up to 1 m b. Use MDI with spacer instead 4. Avoid spirometry 5. Follow infection control recommendations for other aerosol generating procedures

Answer 47

Definition: - Acute or subacute deterioration in sx control that is sufficient to cause distress or risk of health - CM: § Increase in wheeze or SOB § Inc in coughing, esp at night § Lethargy or reduced exercise tolerance § Impairment of daily activities § Poor response to reliever medication

Answer 48

Mild: 1. SABA (2 puffs by pMDI + spacer or 2.5mg by nebulizer q20min for 1 hour) 2. Oxygen (target sats 94-98%) 3. Prednisone 1-2mg/kg po x 3-5d (max 20mg for <2yo, 30mg for 2-5 yo) – if with recurrence of sx in 3-4 hrs 4. If worsening at 1 hour, transfer to high level ICU Severe: 1. Transfer to high level care/ICU 2. O2 by face mask (1L/min) target sats 94-98% 3. Give inhaled SABA 2-6 puffs q20min for first hour, additional 2-3 puffs per hour ipratropium bromide 2 puffs of 90mcg (or 250mcg by nebulizer) q20min for 1 hour only systemic CS methylprednisolone 1mg/kg q6 on day1 Consider MgSO4 nebulized isotonic 150mg 3 doses in the first hour if >2yo 4. Refer to specialist

Answer 49

Disposition Assess for discharge - Sx improved not needing SABA - PEF improving and >60-80% of personal best or predicted - O2sat >94% at room air - Resources at home adequate Arrange for discharge - Reliever: continue prn - Controller: start/ step up - Prednisolone 1-2mkd po continue for 3-5d - Follow up w/in 2-7d Follow-up - Reliever: reduce prn - Controller: continue higher dose for short term (1-2 weeks) or long-term (3 months) depending on reason for exacerbation - Risk factors: check and correct modifiable risk factors that may have contributed to the exacerbation - Review asthma action plan

Answer 50

Respiratory distress – s/sx of abnormal respiratory pattern Respiratory failure – inability of the lungs to provide sufficient oxygen (hypoxic RF) or remove CO2 (ventilatory RF) to meet metabolic demands

Answer 51

Pathophysio - Hypoxic RF results from intrapulmonary shunting and venous admixture or insufficient diffusion of oxygen from alveoli into pulmonary capillaries. From small airway obstruction, inc barrier to diffusion (interstitial edema/fibrosis), alveolar collapse (ARDS, PN, atelectasis, pulmo edema) - Hypercarbic RF is caused by decreased minute alveolar ventilation (TV x RR) from centrally mediated d/o’s of respiratory drive, inc dead space ventilation or obstructive airway ds.

Answer 52

1. Nasal flaring, tachypnea, chest wall retractions, stridor, grunting, dyspnea, wheezing 2. Lethargy, poor cry – signs of exhaustion, hypercarbia, impending respiratory failure 3. Rapid and shallow breathing – indicates decreased lung compliance (PN, pulmonary edema) 4. Slow and deep breathing – indicates obstructive lung disease (asthma, croup) 5. Grunting – decreased FRC (PN, pulmonary edema) and peripheral airway obstruction (bronchiolitis) 6. Hallmark of extrathoracic airway obstruction – inspiratory stridor, suprasternal, intrathoracic and subcostal retractions 7. Hallmark of intrathoracic airway obstruction – prolongation of expiration and expiratory wheezing 8. Alveolar interstitial ds – rapid, shallow respirations, chest wall retractions, grunting

Answer 53

Dx: 1. Pulse oximetry – most common. Indirectly measures arterial Hgb-O2 saturation - Usual target: >95% 2. Capnography (end-tidal CO2 measurement) – determine effectiveness of ventilation and pulmonary circulation 3. ABG – determine acid-base status 4. CXR – to ID etiology of RF

Answer 54

[put table here]

Answer 55

Goal: ensure patent airway and provide necessary support for adequate oxygenation of blood and removal of CO2 1. Oxygen administration – least invasive, most tolerated - Nasal cannula FiO2% O2 delivered = 21% + [(nasal cannula flow x 3)] - Simple mask: 5-10 lpm - Partial rebreather and nonrebreather mask - NIPPV: helps aerate partially atelectatic or filled alveoli, prevent alveolar collapse at end exhalation, and increase FRC - CPAP: high flow nasal cannula delivering 4-16 lpm - Intubation - BiPAP: provided positive pressure during exhalation and inspiration, best for obstructive lung disease 2. ET intubation - When hypoxemia or significant hypoventilation persists despite above. ET internal diameter/size = (age/4)+4 ET depth/length = (age/2) + 12 3. Mechanical ventilation - Apply PEEP to prevent alveolar de-recuitment, small TV, high RR - Indication: PaO2 <60 torr while breathing >60% oxygen - PaCO2 >60torr - pH <7.25 - clinically fatigued, impending exhaustion - goal: provide sufficient O2 and ventilation to ensure tissue viability until disease resolves and minimize complications 4. Weaning - Spontaneous breathing trial (SBT): most objective means of assessing extubation readiness - Patient should be awake, with intact airway reflexes, capable of handling oropharyngeal secretions, and stable hemodynamic status. - With adequate gas exchange: § PaO2 >60mmHg while receiving FiO2 <0.4 and PEEP <5 - If extubatable, shift to CPAP at PEEP 5 - Dexamethasone 0.5mkdose q6 x4 prior to extubation – minimizes risk of postextubation airway obstruction

Answer 56

cough of 2-4 weeks duration

Answer 57

Bronchitis TB Chlamydia pneumonia Mycoplasma pneumonia Rhinosinusitis

Answer 58

Etiology - Usually viral: influenza, parainfluenza, C.diphtheriae

Answer 59

- Tracheobronchial epithelium is invaded by the infectious agent that leads to activation of inflammatory cells and release of cytokines à Inflammation of the large and medium-sized airways of the lungs

Answer 60

- Natural course: 2-3 weeks - Often follows a viral URTI 1. Nonspecific URTI sx 2. After 3-4 d, frequent dry, hacking cough 3. After several days, sputum becomes purulent from leukocyte migration 4. Chest pain exaggerated by coughing 5. Mucus gradually thins within 5-10 days and cough abates 6. Early signs: LG fever, nasopharyngitis, conjunctivitis, rhinitis 7. Late signs: coarse BS, crackles, scattered wheezing

Answer 61

1. Chronic wet cough > 4 weeks 2. No s/sx of other causes of wet/productive cough 3. Resolution of cough after a 2-week course of appropriate oral abx

Answer 62

Dx: Mainly clinical - r/o pneumonia: (-)tachycardia, tachypnea, N chest PE 1. CXR – N or increased bronchial markings

Answer 63

Self-limited. No abx. 1. Rest and inc OFI 2. Humidifiers – shorten course 3. Non-Rx cough and cold meds should not be used in <2yo, and cautioned in 2-11 yo 4. Dextromethorphan – antitussive, for dry cough >4yo. 5. Paracetamol, ibuprofen – for fever/pain 6. PBB – DOC is co-amoxiclav 20-40 mkd q8-12 po x 14d or up to 4 wks.

Answer 64

please see separate deck

Answer 65

Chlamydia pneumonia

Answer 66

The bacteria cause illness by damaging the lining of the respiratory tract including the throat, windpipe, and lungs.

Answer 67

CM: 1. Mild to moderate fever, malaise, cough, pharyngitis 2. Rales and wheezing

Answer 68

Dx: 1. CXR: worse than clinical appearance. Mild diffuse involvement, or lobar infiltrates with small pleural effusion 2. C/S: optimum site is nasopharynx 3. Microimmunofluorescence (MIF): only currently acceptable serologic test. Serum IgM and Ig G. 4. CBC – N WBC, elev eosinophil 5. Elev ESR/ CRP

Answer 69

Tx: 1. Macrolides: Erythromycin 40mkd BIDx10d, Clarithromycin 15mkd BID x 10d, Azithromycin 10mkd on D1, then 5mkd for d2-5 Coughing may persist for weeks even after tx.

Answer 70

Mycoplasma pneumonia

Answer 71

Pathophysio: - M.pneumoniae target the cells of the ciliated respiratory epithelium (bronchi, bronchioles, alveoli) --> ciliostasis and eventual sloughing of cells à cytolytic injury from production of H2O2 and CARDS toxic Community-acquired respiratory distress syndrome (CARDS) toxin associated with more severe/fatal ds § Severe in immunodeficient pxs (hypogammaglobulinemia), sickle cells ds

Answer 72

CM: “walking pneumonia” 1. Gradual onset of headache, malaise, fever, sore throat 2. Followed by LRT sx: hoarseness, nonproductive cough 3. Cough: clinical hallmark of infection. Usually worsens during the 1st week, then gradually resolves within 2wks. Can last to 4 wks 4. Wheezing 5. Generally recover w/o complications 6. N PE, or only dry rales 7. Coryza, GI sx 8. Others: pharyngitis, sinusitis, croup, bronchiolitis

Answer 73

Dx: 1. CXR: interstitial or bronchopneumonia, usually LL. Bilateral diffuse infiltrates, lobar pneumonia, or hilar LNE 2. CBC: N WBC and diff count 3. ESR elev 4. PCR – best method w/ serology 5. C/S – classic “mulberry” colonies 6. Serologic test IgG and IgM – IgM appear after 1st week, then until 6-12mos. IgG >4x on D10-3wks is diagnostic. 7. Cold hemagglutinins

Answer 74

Tx: 1. ABX – Erythromycin 35-50mkd q6/8 Clarithromycin 15mkd po q12 Azithromycin 10mkd OD po x 3d doxycycline 100mg BIDx7-14d 2. CS – for extrapulmonary infection

Answer 75

Complication: 1. CNS disease – most common extrapulmonary site of infection. - Encephalitis, transverse myelitis, aseptic meningitis, GBS, ataxia, Bell palsy, peripheral neuropathy, acute disseminate encephalomyelitis - Occurs 3-23d (mean 10d) after onset of respi sx - Dx: CSF N or mild mononuclear pleocytosis § CSF PCR – from throat swan § MRI – focal ischemic changes, ventriculomegaly, diffuse edema, multifocal white matter inflammatory lesions consistent with postinfectious demyelinating encephalomyelitis 2. Derma – MP urticaria, EM, SJS, Gianotti-Crosti syndrome, erythema nodosum 3. Hema – hemolysis with (+) Coomb’s test and minor reticulocytosis 2-3 weeks after sx onset, thrombocytopenia, aplastic anemia, coagulation defects 4. Arthritis – mono, poly, migratory arthritis 5. Others – hepatitis, pancreatitis, acute GN, pericarditis, myocarditis, RF-like syndrome

Answer 76

Etiology: - S.pneumoniae (30%) - Nontypeable H.influenzae (20%) - M.catarrhalis (20%) - Anaerobes and S.aureus (uncommon)

Answer 77

Pathophysio: - Anything that impairs mucociliary transport or causes nasal obstruction (URTI, AR, smoking) - Sinusitis typically follows a viral URTI à mucosal thickening, edema, inflammation of the paranasal sinuses which block sinus drainage and mucociliary clearance of bacteria favoring bacterial overgrowth

Answer 78

Classification: 1. Acute - <30d 2. Subacute - 1-3mos 3. Chronic - >3mos

Answer 79

CM: 1. Nasal congestion, purulent nasal discharge (x3-4d), fever (>39C), cough >10d w/o improvement 2. Maxillary tooth discomfort and pain or pressure exacerbated by bending forward 3. Headache and facial pain (rare in children) 4. Erythema and swelling of nasal mucosa with purulent nasal discharge 5. Sinus tenderness (adolescents) 6. Transillumination: opaque sinus that transmit light poorly

Answer 80

Complications: 1. Periorbital cellulitis 2. Orbital cellulitis 3. Meningitis 4. Cavernous sinus thrombosis 5. Brain abscess 6. Pott puffy tumor (osteomyelitis of frontal bone) 7. Mucocoeles (chronic inflammatory lesions in the frontal sinuses that expand and displace the eye)

Answer 81

Dx usually clinical 1. Paranasal XR – not diagnostic. Cannot determine etiology, not recommended in otherwise healthy children - Air-fluid level - Opacification of sinuses - Mucosal thickening 2. Sinus aspirate culture – only accurate method of dx, but impractical 3. CBC – usually N

Answer 82

Mgt: 1. ABX: DOC amoxicillin 45mkd BIDx10d (or 7d after resolution of sx) - W/ allergy: cefuroxime 20-30mkd q12 po - Cefixime 8mkd q12-24 po - Co-amoxiclav 80-90 mkd for children w/ risk factors: § Prev. abx in the past 1-3mos § Daycare § <2yo § Failure to respond to amox within 72h § Severe sinusitis - NAGCOM: 1st line: Co-amoxiclav 45-50 mkd po q12 x 10-14d 2nd line: Co-amoxiclav 90 mkd q12 x 10-14d/ Cefuroxime 30mkd q12 x 10d Allergy: Clarithromycin 15mkd q12/ Cefuroxime 30mkd q12 x 10d 2. Refer to ENT – if nonresponsive to abx.

Answer 83

Pertussis, GERD, TEF, Tracheal vascular ring, laryngeal cleft, laryngomalacia

Answer 84

Etiology: - Bordetella pertussis, Bordetella parapertussis - Exclusive pathogen of humans - Natural hx or vax does not provide lifelong immunity

Answer 85

Pathophysio - Bordetella pertussis à pertussis toxin = tracheal cytotoxin à local epithelial damage --> respi sx - Only colonizes ciliated epithelium

Answer 86

7-10 days (4-21days)

Answer 87

CM: 1. Catarrhal stage (1-2 w) – nonspecific sx of LG fever, colds, congestion, sneezing, lacrimation, conjunctival suffusion - Most infectious period 2. Paroxysmal stage (2-6 w) – coughing marks the onset (starts as dry, intermittent and irritative hack) - Cough evolves into paroxysms (hallmark) of 5-10 rapid coughs ending in a high-pitched whoop (forceful inspiratory gasp) “whooping cough” § Inspired air traverses the still partially closed airway - Cyanosis during paroxysmal coughing, posttussive vomiting, and exhaustion, conjunctival hemorrhage, petechiae on upper body - Child looks well in between paroxysms 3. Convalescent stage (>2weeks) – number, severity, and duration of cough episodes diminish Infants (<3mo) – apnea w/ or w/o cough, with gagging, gasping, apnea, cyanosis, apparent life-threatening event

Answer 88

Usually clinical 1. C/S or PCR – posterior nasopharyngeal swab 2. Paired serology 3. CBC – leukocytosis (15-100K cells/uL) with absolute lymphocytosis is characteristic in the catarrhal stage, thrombocytosis 4. CXR – perihilar infiltrate or edema (butterfly

Answer 89

1. Macrolides Erythromycin 40mkd po q6 x 14 d not preferred for <1mo Clarithromycin 15mkd po q12 Azithromycin 10 mkd po x 5d – preferred agent in all age groups 40mkd po q6 x 14 d not preferred for <1mo Clarithromycin 15mkd po q12 Azithromycin 10 mkd po x 5d – preferred agent in all age groups § for infants <1mo. Due to hypertrophic pyloric stenosis with eryth or clarith 2. Aspiration precautions 3. Salbutamol – not recommended. Fussing may trigger paroxysms 4. Droplet precautions and isolation immediately upon dx and until 5d after initiation of tx 5. Admission criteria: a. Infants <3mos old b. Severe 3-6 mos old c. Patients with significant complications

Answer 90

Complications 1. Seizures 2. Encephalopathy 3. Death 4. Apnea 5. Secondary infections (OM, PN) 6. Conjunctival

Answer 91

Prevention: 1. Household contacts & close contacts (daycare) also treated with macrolides 2. Immunization DPT 3. Droplet and standard precautions, isolation – for 5d after starting tx, or 3wks w/o tx

Answer 92

Most common esophageal disorder in children of all ages - GER is physiologic. Passage of gastric contents into the esophagus. - GERD is pathologic: frequent or persistent episodes with complications (esophagitis, respiratory symptoms, FTT, feeding refusal) - 41% of infants aged 3-4mos spit up most of their feedings - <5% of infants age 13-14mos spit up most of their feedings

Answer 93

Pathophysio: - LES is supported by the crura of the diaphragm at the GE junction which have valve-like functions and forms the anti-reflux barrier - Transient LES relaxation (TLESR) is the major mechanism allowing reflux to occur à Retrograde movement of gastric contents across the lower esophageal sphincter (LES) into the esophagus - Gastric distention is the main stimulus for TLESR (straining, coughing, large volume hyperosmolar meals) - GERD is when regurgitation of contents causes complications or contributes to tissue damage or inflammation

Answer 94

Infant reflux at first few mos of life, peaks at 4mos, resolves at 12mos & nearly all at 24 mos - Autosomal dominant genetic predisposition

Answer 95

1. Infants – regurgitation, excessive crying/irritability, vomiting, food refusal, persistent hiccups, abnormal posturing (Sandifer syndrome), impaired QOL 2. Children – impaired QOL, vomiting, esophagitis, persistent/chronic cough, aspiration PN, wheezing, ear infections, stridor, heartburn 3. Adolescents – impaired QOL, esophagitis, dysphagia,

Answer 96

vs. Infant Regurgitation – Rome IV criteria - Must include both of the ff in otherwise healthy infants 3wks-3mos of age: § Regurgitation 2 or more times/d for 3 or more weeks § No retching, hematemesis, aspiration, apnea, FTT, feeding/swallowing difficulties, or abN posturing If there is repetitive regurgitation or vomiting during the first 1-2 WOL, exclude infections, anatomical anomalies, and metabolic disorders Onset of sx after the age of 6 mos or persistence of sx beyond 12 mos raises the possibility of alternative diagnosis to infant GER

Answer 97

Regurgitation started <2 weeks of life or >6mos or persistent after 18mos of life bilious, nocturnal or persistent vomiting chronic or bloody diarrhea hematemesis dysuria seizures dysphagia recurrent pneumonia

Answer 98

abnormal (general or abdominal, neurological, respiratory PE abdominal distention fever failure to thrive/weight loss abnormal muscle tone bulging fontanel or excessive increase of head circumference or micro/macrocephaly abnormal psychomotor development

Answer 99

1. Empiric anti-reflux therapy – trial of high dose PPI Omeprazole 1mkd po od Lansoprazole 15mg po OD 2. Barium study of UGIT – r/o anatomical cause 3. Esophageal pH monitoring – gold standard. Document reflux episodes 4. Esophageal manometry – dysmotility, check LES pressure 5. Endoscopy – erosive esophagitis, strictures, Barrett esophagus. May biopsy, dilate reflux-induced strictures. 6. Gastroesophageal scintigraphy – using 99m-Tc 7. Intraluminal impedance – dx GERD and understand esophageal function, non-acid reflux 8. Laryngotracheobronchoscopy – visualize airway signs of GERD

Answer 100

1. Lifestyle modification – foundation of tx a. Infants:1st line: continue BF, avoid overfeeding, adjust frequency and volume Thicken formula 1 tbsp dry rice cereal per 1 oz MF, commercially thickened MF prone or left lateral position when awake, or upright carried position 2nd line: elimination of cow milk in maternal diet in BF infants 2-4 wks of extensively hydrolyzed proteinbased or amino acid based formula 3rd line: refer to pedia GI OR 4-8 wks trial of acid suppression (PPI, H2RA if PPI not available) b. Avoid acidic/spicy food, juice, alcohol, caffeinated and carbonated drinks c. Hypoallergenic diet d. Weight reduction e. Avoid smoking f. Positioning: elevate head during sleep, left lateral decubitus 2. PPI – current standard of care Omeprazole 1mkd po od for upto 8wks Lansoprazole 15mg po OD Esomeprazole 10mg (<12yo), 20mg (>12yo) od po 3. Others: antacids, H2 blockers, prokinetic agents (metoclopramide) 4. Fundoplication – for intractable GERD, refractory esophagitis & strictures, CPD

Answer 101

Abnormal connection (fistula) between the esophagus and trachea

Answer 102

Types of TEF 1. Type A (80%) – isolated EA, pure EA w/o TEF 2. Type B (<1%) – EA with proximal TEF 3. Type C (87%) – EA with distal TEF - Most common type - Esophagus ends blindly 10-20cm from the nares - Upper esophagus ends in a blind pouch. The distal esophagus communicates with the posterior trachea 4. Type D (<1%) – EA with double TEF 5. Type E (4%) – isolated TEF

Answer 103

Risk factors: 1. Advanced maternal age, European 2. Obesity, poor, smoking

Answer 104

CM: 1. At birth – frothing/bubbling at mouth and nose; respiratory distress, cough, cyanosis 2. Infant – unable to handle secretions with subsequent salivation and aspiration of pharyngeal contents due to esophageal obstruction, requires frequent suctioning 3. Feeding exacerbates sx à regurgitation, aspiration

Answer 105

Dx: 1. Inability to pass NGT or OGT in NBs + early-onset respiratory distress 2. CXR – coiled NGT/OGT in the esophageal pouch, airdistended stomach 3. 50% with associated anomalies (VATER/VACTERL): Vertebral, Anorectal, Cardiac, Trachea, Esophagus, Renal/Radial, Limb syndrome

Answer 106

Mgt: 1. Supportive a. Maintain a patent airway b. Pre-operative proximal pouch decompression to prevent aspiration of secretions c. ABX for PN ampicillin 50mg/kg or benzylpenicillin 50,000 U/kg q6h x 5 d + Gentamicin 7.5mg/kg OD x 5d d. Prone positioning to reduce regurgitation & esophageal suctioning 2. Surgery – surgical ligation of TEF and primary end-toend anastomosis of the esophagus via right-sided thoracotomy

Answer 107

Prognosis : >90% survival rate Complications: GERD, delayed gastric emptying

Answer 108

- Usually occur in 1st year of life - At birth, acute respiratory distress - Congenital vascular encirclement of the trachea and esophagus - Double aortic arch: MC sx’c vascular ring

Answer 109

1. Asymptomatic, wheezing, stridor, recurrent URTI and/or dysphagia 2. Hyperextended neck to alleviate respiratory distress 3. Exacerbated by neck flexion 4. Reflex apnea during feeding

Answer 110

Dx: 1. CXR – evaluate pulmo pathology and sidedness. compression of the trachea and hyperinflation or atelectasis of some of the lobes of either lung 2. Echocardiogram – ID anatomy 3. Contrast CT angiogram – define anatomy 4. Bronchoscopy – best method to define degree and extent of stenosis/ tracheal compression

Answer 111

Mgt: 1. Tracheal resection of short segment stenosis/slide tracheoplasty for long segment stenosis

Answer 112

Insufficient tracheal cartilage to maintain airway patency throughout the respiratory cycle - Usually infants, M:F 2:1

Answer 113

CM: 1. Low-pitched monophasic wheezing during expiration, loudest at trachea 2. Persistent respiratory congestion

Answer 114

Dx: 1. Flexible/rigid bronchoscopy – gold standard. Observe airway collapsing and opening 2. PFT – dec. peak flow, flattening of flow-volume loop 3. MRI/MRA, CT – reveal abnormal shape of the trachea as the apposition of the walls, “expiratory frown shapes”

Answer 115

Mgt 1. Expectant observation. Usually resolves by 3yo. 2. Postural drainage to clear secretions 3. Nebulization: ipratropium bromide Don’t give Salbutamol – decrease airway tone à exacerbate loss of airway patency 4. CPAP Prognosis: Excellent – improves as child grows due to increase in airway diameter (resolved at 3yo)

Answer 116

- Result when the septum between the esophagus and trachea fail to develop fully, leading to a common channel defect between the pharyngoesophagus and laryngotracheal lumen, making laryngeal closure incompetent during swallowing/reflux.

Answer 117

CM: 1. Stridor, choking, cyanosis, aspiration of feedings, recurrent chest infections

Answer 118

1. laryngoscopy – visualize laryngeal cleft and esophagus.

Answer 119

surgical repair

Answer 120

Most common congenital laryngeal anomaly - Most common cause of stridor in children

Answer 121

Patho: - Due to decreased laryngeal tone leading to supraglottic collapse during inspiration

Answer 122

CM: 1. Stridor – low pitched, inspiratory, exacerbated by exertion – crying, agitation, feeding 2. Sx at first 2 weeks of life, increasing in severity for 6 mos

Answer 123

Dx: 1. Flexible laryngoscopy – gold standard. Laryngeal cartilage collapsing on inspiration. Directly assess the dynamic collapse of the supraglottic airway during awake respiration. 2. CXR – visualize swallowing mechanism. Modified barium swallow for infants

Answer 124

Tx: 1. Expectant observation – most sx resolve spontaneously as child and airway grows 2. Surgery – supraglattoplasty if with severe respiratory distress, FTT.